Jos F Frencken1,2, Lottie van Baal2, Teus H Kappen3, Dirk W Donker2, Janneke Horn4, Tom van der Poll5,6, Wilton A van Klei3, Marc J M Bonten1,7, Olaf L Cremer2. 1. 1 Julius Center for Health Sciences and Primary Care. 2. 2 Department of Intensive Care Medicine. 3. 3 Department of Anesthesiology, and. 4. 4 Department of Intensive Care and. 5. 5 Center for Experimental and Molecular Medicine, and. 6. 6 Division of Infectious Diseases, Academic Medical Center, Amsterdam, the Netherlands. 7. 7 Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, the Netherlands; and.
Abstract
Rationale: Myocardial injury, as reflected by elevated cardiac troponin levels in plasma, is common in patients with community-acquired pneumonia (CAP), but its temporal dynamics and etiology remain unknown. Objectives: Our aim was to determine the incidence of troponin release in patients with CAP and identify risk factors that may point to underlying etiologic mechanisms. Methods: We included consecutive patients admitted with severe CAP to two intensive care units in the Netherlands between 2011 and 2015. High-sensitivity cardiac troponin I was measured daily during the first week. We used multivariable linear regression to identify variables associated with troponin release on admission, and we used mixed-effects regression to model the daily rise and fall of troponin levels over time. Results: Of 200 eligible patients, 179 were included, yielding 792 observation days. A total of 152 (85%) patients developed raised troponin levels greater than 26 ng/L. Baseline factors independently associated with troponin release included coronary artery disease (176% increase; 95% confidence interval [CI], 11-589), smoking (248% increase; 95% CI, 33-809), and higher Acute Physiology and Chronic Health Evaluation IV score (2% increase; 95% CI, 0.8-3.3), whereas Staphylococcus aureus as a causative pathogen was protective (70% reduction; 95% CI, 18-89). Time-dependent risk factors independently associated with daily increase in troponin concentrations included reduced platelet count (2.3% increase; 95% CI, 0.6-4), tachycardia (1.5% increase; 95% CI, 0.1-2.9), hypotension (6.2% increase; 95% CI, 2.1-10.6), dobutamine use (44% increase; 95% CI, 12-85), prothrombin time (8.2% increase; 95% CI, 0.2-16.9), white cell count (1.7% increase; 95% CI, 0-3.5), and fever (22.7% increase; 95% CI, 0.1-49.6). Conclusions: Cardiac injury develops in a majority of patients with severe CAP. Myocardial oxygen supply-demand mismatch and activated inflammation/coagulation are associated with this injury. Clinical trial registered with www.clinicaltrials.gov (NCT01905033).
Rationale: Myocardial injury, as reflected by elevated cardiac troponin levels in plasma, is common in patients with community-acquired pneumonia (CAP), but its temporal dynamics and etiology remain unknown. Objectives: Our aim was to determine the incidence of troponin release in patients with CAP and identify risk factors that may point to underlying etiologic mechanisms. Methods: We included consecutive patients admitted with severe CAP to two intensive care units in the Netherlands between 2011 and 2015. High-sensitivity cardiac troponin I was measured daily during the first week. We used multivariable linear regression to identify variables associated with troponin release on admission, and we used mixed-effects regression to model the daily rise and fall of troponin levels over time. Results: Of 200 eligible patients, 179 were included, yielding 792 observation days. A total of 152 (85%) patients developed raised troponin levels greater than 26 ng/L. Baseline factors independently associated with troponin release included coronary artery disease (176% increase; 95% confidence interval [CI], 11-589), smoking (248% increase; 95% CI, 33-809), and higher Acute Physiology and Chronic Health Evaluation IV score (2% increase; 95% CI, 0.8-3.3), whereas Staphylococcus aureus as a causative pathogen was protective (70% reduction; 95% CI, 18-89). Time-dependent risk factors independently associated with daily increase in troponin concentrations included reduced platelet count (2.3% increase; 95% CI, 0.6-4), tachycardia (1.5% increase; 95% CI, 0.1-2.9), hypotension (6.2% increase; 95% CI, 2.1-10.6), dobutamine use (44% increase; 95% CI, 12-85), prothrombin time (8.2% increase; 95% CI, 0.2-16.9), white cell count (1.7% increase; 95% CI, 0-3.5), and fever (22.7% increase; 95% CI, 0.1-49.6). Conclusions: Cardiac injury develops in a majority of patients with severe CAP. Myocardial oxygen supply-demand mismatch and activated inflammation/coagulation are associated with this injury. Clinical trial registered with www.clinicaltrials.gov (NCT01905033).
Authors: Raymundo Vera-Pineda; Edgar Francisco Carrizales-Sepulveda; Adrian Camacho-Ortiz; Laura Nuzzolo-Shihadeh; Francisco Cruz-Ramos; Alejandro Ordaz-Farias; Mario Alberto Benavides-Gonzalez; Gabriel Carranza-Villegas Journal: Cardiol Res Date: 2020-06-03
Authors: Peter Jirak; Robert Larbig; Zornitsa Shomanova; Elisabeth J Fröb; Daniel Dankl; Christian Torgersen; Nino Frank; Magdalena Mahringer; Dominyka Butkiene; Hendrik Haake; Helmut J F Salzer; Thomas Tschoellitsch; Michael Lichtenauer; Alexander Egle; Bernd Lamprecht; Holger Reinecke; Uta C Hoppe; Rudin Pistulli; Lukas J Motloch Journal: ESC Heart Fail Date: 2020-12-17